Akademik Veri Yönetim Sistemi
PHARMACOLOGICAL RESEARCH, cilt.38, sa.3, ss.173-178, 1998 (SCI-Expanded)
The purpose of the present study was to investigate a possible role of platelet activating factor (PAF) in ischaemic preconditioning (PC). Since both PC and PAF act through protein kinase C (PKC), PAF could play a role in PC. To test this hypothesis, anaesthetized, open-chest male rats were subjected to four different protocols. Group I was subjected to 30 min of left coronary artery occlusion. In Group II, WEB 2086 (10 mg kg(-1) i.v. bolus +1 mg kg(-1) h(-1) i.v. infusion) a selective PAF antagonist was given to non-preconditioned rats 23 min before the 30-min occlusion period. In Group III and IV ischaemic PC was elicited by one cycle of 3 min occlusion and 5 min reperfusion and also in Group IV, WEB 2086 (10 mg kg(-1) i.v. bolus +1 mg kg(-1) h(-1) i.v. infusion) was given 23 min before the 30 min occlusion period. Ventricular ectopic beats (VEB), ventricular tachycardia (VT), and ventricular fibrillation (VF) that occurred during 30 min occlusion were determined. WEB 2086 administration or PC reduced the VEBs significantly. Incidence of VT and VF were not affected by WEB 2086 compared with control values, although PC decreased the incidence of VT and VF. WEB 2086 administration did not attenuate PC-induced improvement of arrhythmia parameters. These data demonstrated that a specific PAF antagonist, WEB 2086 did not abolish PC-induced protection against arrhythmias. (C) 1998 The Italian Pharmacological Society.